JORGE ELIAS KALIL FILHO

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Departamento de Clínica Médica, Faculdade de Medicina - Docente
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/19 - Laboratório de Histocompatibilidade e Imunidade Celular, Hospital das Clínicas, Faculdade de Medicina - Líder

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Assunto: Immunology ×

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Agora exibindo 1 - 10 de 235
  • conferenceObject
    Immune Responses Of CVID Patients To COVID-19 Vaccines
    (2023) MEDEIROS, Giuliana Xavier de; FERREIRA, Loisi de Carvalho Pereira; MAGAWA, Jhosiene Yukari; KURAMOTO, Andreia; SASAHARA, Greyce Luri; FERREIRA, Marcelo; BARROS, Myrthes Maragna Toledo; KALIL, Jorge; MARINHO, Ana Karolina Barreto Berselli; CUNHA-NETO, Edecio; SANTOS, Keity Souza; KOKRON, Cristina
  • article 20 Citação(ões) na Scopus
    Drug-induced anaphylaxis: is it an epidemic?
    (2018) GIAVINA-BIANCHI, Pedro; AUN, Marcelo V.; KALIL, Jorge
    Purpose of reviewThe present review addresses the epidemiology, analyzes the current data and promotes global awareness of drug-induced anaphylaxis.Recent findingsAnaphylaxis is a medical emergency that may cause death! In the last decade, studies have shown an increasing incidence and prevalence of anaphylaxis.SummaryDrug-induced anaphylaxis fatalities have increased, and this syndrome remains underdiagnosed and undertreated.
  • conferenceObject
    Inhaled corticoids in asthmatic patients: effect on body mass index and spirometry
    (2018) PACHECO, Rosilane dos Reis; ANDRADE, Mayra Coutinho; PEDROSO, Natalia Falci; TAKEJIMA, Priscila; AUN, Marcelo V.; KALIL FILHO, Jorge Elias; GIAVINA-BIANCHI, Pedro; AGONDI, Rosana C.
  • article 46 Citação(ões) na Scopus
    Disease Tolerance and Pathogen Resistance Genes May Underlie Trypanosoma cruzi Persistence and Differential Progression to Chagas Disease Cardiomyopathy
    (2018) CHEVILLARD, Christophe; NUNES, Joao Paulo Silva; FRADE, Amanda Farage; ALMEIDA, Rafael Ribeiro; PANDEY, Ramendra Pati; NASCIMENTO, Marilda Savoia; KALIL, Jorge; CUNHA-NETO, Edecio
    Chagas disease is caused by infection with the protozoan Trypanosoma cruzi and affects over 8 million people worldwide. In spite of a powerful innate and adaptive immune response in acute infection, the parasite evades eradication, leading to a chronic persistent infection with low parasitism. Chronically infected subjects display differential patterns of disease progression. While 30% develop chronic Chagas disease cardiomyopathy (CCC)-a severe inflammatory dilated cardiomyopathy-decades after infection, 60% of the patients remain disease-free, in the asymptomatic/indeterminate (ASY) form, and 10% develop gastrointestinal disease. Infection of genetically deficient mice provided a map of genes relevant for resistance to T. cruzi infection, leading to the identification of multiple genes linked to survival to infection. These include pathogen resistance genes (PRG) needed for intracellular parasite destruction, and genes involved in disease tolerance (protection against tissue damage and acute phase death-DTG). All identified DTGs were found to directly or indirectly inhibit IFN-gamma production or Th1 differentiation. We hypothesize that the absolute need for DTG to control potentially lethal IFN-gamma PRG activity leads to T. cruzi persistence and establishment of chronic infection. IFN-gamma production is higher in CCC than ASY patients, and is the most highly expressed cytokine in CCC hearts. Key DTGs that downmodulate IFN-gamma, like IL-10, and Ebi3/IL27p28, are higher in ASY patients. Polymorphisms in PRG and DTG are associated with differential disease progression. We thus hypothesize that ASY patients are disease tolerant, while an imbalance of DTG and IFN-gamma PRG activity leads to the inflammatory heart damage of CCC.
  • conferenceObject
    Chronic Spontaneous Urticaria: Response to Antileukotriene
    (2017) LOPES, Mariele Morandin; SALLES, Pamella Diogo; DANTAS, Paula; KALIL, Jorge; MOTTA, Antonio Abilio; AGONDI, Rosana Camara
  • article 30 Citação(ões) na Scopus
    Myocardial gene and protein expression profiles after autoimmune injury in Chagas' disease cardiomyopathy
    (2011) CUNHA-NETO, Edecio; TEIXEIRA, Priscila C.; FONSECA, Simone G.; BILATE, Angelina M.; KALIL, Jorge
    One third of the 16 million of individuals infected by the protozoan Trypanosoma cruzi in Latin America eventually develop chronic Chagas' disease cardiomyopathy (CCC), an inflammatory dilated cardiomyopathy with shorter survival than non-inflammatory cardiomyopathies. The presence of a T cell-rich mononuclear inflammatory infiltrate and the relative scarcity of parasites in the heart suggested that chronic inflammation secondary to the autoimmune recognition of cardiac proteins could be a major pathogenetic mechanism. Sera from CCC patients crossreactively recognize cardiac myosin and T. cruzi protein B13. T cell clones elicited from peripheral blood with T. cruzi B13 protein or its peptides could crossreactively recognize epitopes from cardiac myosin heavy chain. Likewise, CD4+ T cell clones infiltrating CCC myocardium crossreactively recognize cardiac myosin and T. cruzi protein B13, and intralesional T cell lines produce the inflammatory cytokines IFN-gamma and TNF-alpha. Conversely, IFN-gamma-induced genes and chemokines were found to be upregulated in CCC heart samples, and IFN-gamma is able to induce cardiomyocyte expression of atrial natriuretic factor, a key member of the hypertrophy/heart failure signature. Proteomic analysis of CCC heart tissue showed reduced expression of the energy metabolism enzymes. It can be hypothesized that cytokine-induced modulation of cardiomyocyte gene/protein expression may be a novel disease mechanism in CCC, in addition to direct inflammatory damage.
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    Descriptive Review of Clinical Data from 186 Records of Outpatients with IgA Deficiency Accompanied at a Quaternary Hospital in Brazil
    (2014) MENDONCA, L.; MASCARENHAS, F.; COHON, A.; KOKRON, C.; GRECCO, O.; KALIL, J.; BARROS, M.
  • conferenceObject
    Anaphylaxis during skin prick test with aeroallergen extract: Case report
    (2021) OLIVEIRA, I. A.; PRADO, A. I. F.; ALBERTO, N. E. S.; MENECHINO, N. T. C.; KALIL, J.; GIAVINA-BIANCHI, P.; AGONDI, R. C.
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    Whole exome sequencing of Chagas disease cardiomyopathy families reveals accumulation of rare variants in mitochondrial and inflammation-associated genes
    (2019) CUNHA-NETO, E.; MARQUET, S.; FRADE, A. Farage; FERREIRA, A. Mota; OUARHACHE, M.; IANNI, B.; FERREIRA, L. Rodrigues Pinto; RIGAUD, V. Oliveira-Carvalho; ALMEIDA, R. Ribeiro; CANDIDO, D.; TORRES, M.; GALLARDO, F.; FERNANDES, R.; MADY, C.; BUCK, P.; CARDOSO, C.; SANTOS-JUNIOR, O. R.; OLIVEIRA, L. C.; OLIVEIRA, C. D. L.; NUNES, M. do Carmo; ABEL, L.; KALIL, J.; RIBEIRO, A. L. P.; SABINO, E. C.; CHEVILLARD, C.
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    Evaluation of autologous serum skin test positivity and autoantibodies status in patients with chronic spontaneous urticaria (CSU)
    (2019) PEREIRA, G. D. F.; MAMEDE, L. D. Q.; GOMES, L. S.; MAIA, L. P.; KALIL, J.; MOTTA, A. A.; BARROS, M. T.; AGONDI, R. C.